Post Op complications in general surgery

“Two things surgeons fears the most are God
and peritonitis”
- Henry Mondor

POST OPERATIVE COMPLICATIONS
Student: Maj Adil A Kalam
Guide: Lt Col SK Dey
“A surgeon who has no complications is
either not operating or is being economical
with the truth”

INTRODUCTION
• The cost
• Lost work productivity
• Disruption of family life
• Stress to employers and society in general.
• Functional results -compromised
(preoperative level of function.)
• Anticipating an uneventful operation but
compromised by the complication

• Patient Factors
• Surgeon/Technical factors
• Disease factors/Surgery
• Immediate
• Early
• Delayed/Late

Avoiding complications- Preop
• Careful preoperative screening.
• Nutritional status
• Health of the heart and lungs.
• Appropriate operation
• Timing of the operation-elective vs urgent
• Weight
• Preoperative consultation from a cardiologist
or pulmonary specialist

• Handle tissues gently, dissect meticulously,
and honor tissue planes.
• Avoid the temptation to rush, cut corners, or
accept marginal technical results.
• Judicious use of antibiotics and other
preoperative medications
Avoiding complications- Intraop

• Compulsive postoperative surveillance
• Be vigilant and seek postoperative complications at an
early stage,
– checks all wounds
– evaluates intake and output
– checks temperature profiles,
– ascertains what the patient’s activity levels have been,
– Evaluates nutritional status
– checks pain levels.
• Deviations from the normal course- Experience
Avoiding complications- Postop

OUTLINE
1. Surgical Wound Complications
2. Complications of Thermal Regulation
3. Respiratory Complications
4. Cardiac Complications
5. Renal and Urinary Tract Complications
6. Endocrine Gland Dysfunction
7. Gastrointestinal Complications
8. Hepatobiliary Complications
9. Neurologic Complications
10. Ear, Nose, and Throat Complications

SURGICAL WOUND COMPLICATIONS
• Seroma
• Haematoma
• Acute Wound Failure (Dehiscence)
• Surgical Site Infection (Wound Infection)

SEROMA
• Collection-liquefied fat, serum,& lymphatic fluid
• Most benign complication
• Large skin flaps
– Mastectomy
– Axillary Dissection
– Groin Dissection
– Large ventral Hernia repairs
• Swelling/discomfort/drainage
• Prevention- suction drain under flaps

• Treatment
– Aspiration+Pressure bandage
– Recumilating after 2 aspirations- Open and pack
– Synthetic mesh- Open and suction drain
– Infected seroma- Open
– Mesh Explantation?
SEROMA

“The most important clotting factor is the
surgeon”-Moshe schein
“Operative atlases never bleed”
HEMATOMA

HEMATOMA
• Abnormal collection of blood
• More potential for secondary infection
• Causes
 inadequate hemostasis
depletion of clotting factors
presence of coagulopathy
Diseases and medications that contribute to
coagulopathy

HEMATOMA
• PRESENTATION
 Varies with size, location, presence of infection
 Expanding, unsightly swelling or pain in area of surgical
incision
Neck- compromise of airway
Retroperitonium- paralytic ileus, anaemia, ongoing
bleeding
Extremity and abdominal cavity- compartment syndrome
• Physical examination- localized swelling with
purplish blue discolouration, may be tender.

HEMATOMA
• PREVENTION
– correcting clotting abnormalities
– Discontinuing medications that alter coagulation
• Risk of bleeding vs Thromboembolic events
• Discontinue VKA 4-5 days before surgery -INR to be
<1.5
• If INR>1.5- low dose Vit K orally(1-2mg)
• Bridging anticoagulation
– IV UFH-discontinued 4 hrs before surgery
– Therapeutic dose LMWH S/C- 16-24 hrs before surgery
• VKA- resumed 12-24 hrs after surgery(2-3 days for

• Acetyl salicylic acid/Clopid-withhold 6-7 d
begore surgery
• Antiplatelet therapy resumed approximately
24 hrs after surgery
• Emergency setting!
– VKA-FFP, Low dose iv or oralVit K
HEMATOMA

HEMATOMA
• Evaluation- assessment of risk factors and
coagulation parameters
• Small hematoma- eventually resorbs
• Retroperitoneal hematoma-expectant waiting
after associated coagulopathy
• Expanding hematoma in neck- evacuated in
the operating room after securing airway if
there is any respiratory compromise.

ACUTE WOUND FAILURE(DEHISCENCE)
“Abdominal wall closure- if it looks all right, it’s
too tight- if it looks too lose, it’s all right”
- Matt Oliver

• Postoperative separation of the abdominal
musculoaponeurotic layers
• Risk of evisceration, repeat dehiscence, surgical
wound infection, incisional hernia formation.
• 1-3% patients undergoing abdominal operations
• Can be predisposed by hematoma and infection

Factors associated with wound dehiscence
• Technical error in fascial closure
• Emergency surgery
• Intra-abdominal infection
• Advanced age
• Wound infection, hematoma, and seroma
• Elevated intra-abdominal pressure
• Obesity
• Long-term corticosteroid use
• Previous wound dehiscence
• Malnutrition
• Radiation therapy and chemotherapy
• Systemic disease (uremia, diabetes mellitus)

ACUTE WOUND FAILURE(DEHISCENCE
• PRESENTATION
 Sudden dramatic drainage of large volume of clear, salmon
coloured fluid preceeds dehiscence in 25%patients
Ripping sensation
• PREVENTION- good fascial closure
• TREATMENT
Small dehiscence- conservatively with saline moistened gauze
packing, use of abdominal binder.
Large segment of wound that is open to the omentum and
intestines, if there is peritonitis or interstitial leak-Explore
Management of infection

• Management of incision
Fascia strong and intact- primary closure
Fascia Infected and necrotic-debridement
Can be Closed with retention sutures, use of
prosthetic material may be preferred
Closure with an absorbable mesh- associated with
fistula formation and hernia formation repair.
Skin graft applied after granulation of wound
Hernia-removal of skin graft and permanent
prosthesis or dermabration of skin graft followed by
facial closure using component separation

SURGICAL SITE INFECTION
(WOUND INFECTION)
• The surgical wound encompasses the area of
the body, internally and externally, that
involves the entire operative site.
• Wounds are generally categorized as follows:
1. Superficial-skin and subcutaneous tissue
2. Deep-fascia and muscle
3. Organ space-internal organs included in operation

(WOUND INFECTION)
• PRESENTATION
5-6 days post operatively, may vary
Approximately 80-90%of all post operative infections
occur within 30 days after surgery.
• SSIs are accompanied by
Erythema
Tenderness
Occassionally discharge
Leucocytosis
Low grade fever

According
to the
relative risk
of SSI
occurring

(WOUND INFECTION)
• Prevention
Stop smoking at least 30 days before surgery
Blood glucose levels maintained
Malnourished patients given nutritional
supplements
Obese patients encouraged to lose weight
Bowel preparation for major abdominal surgeries
Perioperative antibiotiics

(WOUND INFECTION)
•preoperative dose, intraoperative doses approximately 4 hours apart, and two
postoperative doses appropriately spaced.
•prophylactic -intravenously within 30 minutes before the incision-therapeutic
tissue levels -when the wound exposed to bacterial contamination

(WOUND INFECTION)
1. Careful handling of tissues
2. Meticulous dissection, hemostasis, and débridement
of devitalized tissue
3. Compulsive control of all intraluminal contents
4. Preservation of blood supply of the operated organs
5. Elimination of any foreign body from the wound
6. Maintenance of strict asepsis
7. Thorough drainage and irrigation with warm saline of
any pockets of purulence in the wound
8. Patient kept in euthermic state and fluid-resuscitated
9. Expressing a decision about closing the skin or packing
the wound at the end of the procedure

(WOUND INFECTION)
• TREATMENT
Depends on depth of infection
Skin staples removed and a cotton tip applicator easily
passed into the wound, with efflux of purulent material
and puss. Wound explored.
If fascia intact- debridement of any non viable tissue-
irrigated-packed
If widespread cellulitis and significant signs of infection-
IV antibiotics.
Wound cultures are controversial.
Doubtful about amount of contamination- close
observation of wound followed by closure of skin or

COMPLICATIONS OF THERMAL REGULATION
• Hypothermia
• Malignant Hyperthermia
• Postoperative Fever

HYPOTHERMIA
• CAUSES
Preoperatively, intraoperatively or postoperatively
Trauma patient with injuries in a cold environment
Paralysis-because of loss of shiver mechanism
In patients undergoing rapid resuscitation with cool IV fluids,
transfusions, or inracavitary irrigation with cold irrigant.
Patients undergoing prolonged surgical procedures.
Almost all anesthetics impair thermoregulation.
Propofol- vasodilation- redistribution hypothermia
Postoperatively
o Cool ambient room temperature
o Rapid administration of IV fluids or blood
o Failure to keep patients covered

HYPOTHERMIA
• PRESENTATION
Intense cold sensation and shivering.
Associated with profound affects on CVS, coagulation, wound
healing, and infection.
Core temperature <35 degree Celsius
o Increased norepinephrine level, vasoconstriction and elevated blood
pressure.
o Increases incidence of postoperative ischemia and ventricular
tachyarrhythmia.
Poor perfusion of peripheral organs and tissues.
Increased risk of bleeding
Poor wound healing and infection.
Relative diuresis, compromised hepatic function
Severe cases- significant cardiac slowing and may be comatose, with
low blood pressure, bradycardia, and a very low respiratory rate.

HYPOTHERMIA
• PREVENTION
Monitoring core temperature
Sites
o Pulmonary artery blood
o Tympanic membrane
o Esophagus and pharynx
o Rectum
o Urinary bladder
Keeping patient warm by increasing the ambient
temperature and using heated humidifiers and warmed
IV fluids.

HYPOTHERMIA
• TREATMENT
Attention must be directed toward rewarming by the
following methods:
1. Immediate placement of warm blankets as well as
currently available forced-air warming devices
2. Infusion of blood and IV fluids through a warming device
3. Heating and humidifying inhalational gases
4. Peritoneal lavage with warmed fluids
5. Rewarming infusion devices with an arteriovenous system
6. In rare cases, cardiopulmonary bypass
Special attention must be paid to cardiac monitoring during
the rewarming process.

MALIGNANT HYPERTHERMIA
• Life-threatening hypermetabolic crisis
manifested during or after exposure to a
triggering general anesthetic in susceptible
individuals.
• Autosomal dominant disease with variable
penetrance
• Mutation resulting in altered calcium
regulation in skeletal muscle

Halogenated inhalational anesthetic agents (e.g., halothane, enflurane, isoflurane,
desflurane, and sevoflurane) and depolarizing muscle relaxants (e.g., succinylcholine,
suxamethonium) cause an increase in the myoplasmic Ca2+ concentration.
Exposed to
triggering
anesthetic
Abnormal release
of calcium
Prolonged activation of
muscle filaments
culminating in rigidity
and hyper metabolism
Uncontrolled
glycolysis and
aerobic metabolism
Cellular hypoxia,
progressive lactic
acidosis, and
hypercapnia
Continuous muscle
activation with ATP
Excessive
generation of
heat
Myocyte death and
rhabdomyolisis result in
hyperkalemia and
myoglobinuria

MALIGNANT HYERTHERMIA
• PREVENTION
– Identify risked individuals before surgery- history,
tendency to develop fever, muscular disease,
intolerance to caffeine.
– Caffeine and halothane contraction test
– Trigger free anaesthetic-barbiturate,
benzodiazepine, opiod, propofol, ketamine, non
depolarizing neuromuscular blocker.

MALIGNANT HYERTHERMIA
• PRESENTATION
– Abortive form of MH (e.g., tachycardia, arrhythmia,
increased temperature, acidosis).
– Other patients, after intubation with succinylcholine-- loss
of twitches on neuromuscular stimulation and develop
muscle rigidity.
– An inability to open the mouth-masseter spasm 
pathognomonic early sign-indicates susceptibility to MH.
– Tachypnea, hypercapnia, skin flushing, hypoxemia,
hypotension, electrolyte abnormalities, rhabdomyolysis,
and hyperthermia.

• MANAGEMENT
DISCONTINUE
TRIGGERING
ANAESTHETIC
HYPERVENTILATE
WITH 100
PERCENT OXYGEN
ADMINISTER
ALTERNATIVE
ANAESTHESIA
TERMINATE
SURGERY
DANTROLENE,
2.5MG/KG, AS A
BOLUS AND REPEAT
EVERY 5 MINUTES
1-2MG/KG UNTIL
NORMALISATION OR
DISSAPEARANCE OF
SYMPTOMS
CHECK AND MONITOR
ARTERIAL BLOOD GAS AND
CREATINE KINASE,
ELECTROLYTE, LACTATE AND
MYOGLOBIN LEVELS.
MONITOR ECG,
VITAL SIGNS AND
URINE OUTPUT
ADJUNCTIVE AND
SUPPORTIVE
MEASURES ARE
CARRIED OUT

DANTROLENE!
• DANTROLENE is a muscle relaxant.
– In the solution form- highly irritating to the vein- administered in a large
vein.
– IV dantrolene blocks up to 75% of skeletal muscle contraction and never
causes paralysis.
– Plasma elimination half-life is 12 hours.
– Metabolized in the liver to 5-hydroxydantrolene-also acts as a muscle
relaxant.
– Side effectsmuscle weakness, phlebitis, respiratory failure, GI
discomfort, hepatotoxicity, dizziness, confusion, and drowsiness.
• AZUMOLENE, is 30 times more water-soluble than and equipotent
to dantrolene in the treatment of MH; similar to dantrolene, it does
not affect the heart. Its main side effect is marked pulmonary
hypertension. However, azumolene is not in clinical use at this time.

ADJUNCTIVE AND SUPPORTIVE MEASURES

Volatile vaporizers are removed from the anesthesia machine.
Carbon dioxide canisters, bellows, and gas hoses are changed.
Surface cooling is achieved with ice packs and core cooling with cool
parenteral fluids.
Acidosis is monitored and treated with sodium bicarbonate.
Arrhythmias are controlled with beta blockers or lidocaine.
Urine output more than 2 mL/kg/hr is promoted; furosemide (Lasix) or
mannitol and an infusion of insulin and glucose (0.2 U/kg in a 50% glucose
solution) are given for hyperkalemia, hypercalcemia, and myoglobulinuria.
Patient transferred to ICU to monitor for recurrence

POST OPERATIVE FEVER
• Fever is an increase in core temperature, the
modulation of which is managed by the
anterior hypothalamus.
• Stimulation of production of cytokines.
• The inflammatory responseproduction of
various mediators induce a febrile
inflammatory response, also known as
systemic inflammatory response syndrome.

• CAUSES

• The most common infections are health care–associated
infections—SSI, urinary tract infection (UTI), intravascular
catheter–related bloodstream infection (CR-BSI), and
pneumonia.
• UTI
– A major predisposing factor-presence of a urinary catheter-
increased duration of catheterization (>2 days).
– Endogenous bacteria (colonic flora, most common E. coli) are the
most common source.
– Candiduria accounts for approximately 10% of nosocomial UTIs.
– The presence of an indwelling catheter, diabetes mellitus, use of
antibiotics, advanced age, and underlying anatomic urologic
abnormalities are risk factors for candiduria.

POST OPERATIVE FEVER-CR-BSI
• The use of central venous catheters
• Microorganisms that colonize t he hubs or from
contamination of the injection site of the CVC(intraluminal
source) or skin (extraluminal source).
• Coagulase- staphylococci, hospital acquired bacteria (e.g.,
MRSA, multidrug-resistant gram-bacilli, fungal species
[Candida albicans]) –mc organisms .
• Metastatic infections (endocarditis)-rre but serious
complication
• Risk factors -duration of CVC, patient location (outpatient
versus inpatient), type of catheter, number of lumens and
manipulations daily, emergent placement, need for TPN,
presence of unnecessary connectors.

PRESENTATION
• High fever that fluctuates or is sustained and
that occurs 5 to 8 days after surgery is more
worrisome.
• In the first 48 to 72 hours after abdominal
surgery-atelectasis-the cause of the fever.
• Clostridial or streptococcal SSIs-fever within
the first 72 hours of surgery.

EVALUATION
• Six “W”’s
o Wind(lungs)
o Wound
o Water(urinary tract)
o Waste(lower GI tract)
o Wonder drugs(eg. Antibiotics)
o Walker(eg. Thrombosis)
• Symptoms indicate organ system involved
o Sputum-pneumonia
o Frequency, dysuria- UTI
o Watery foul smelling diarrhea-infection with C.difficile
o Pain in the calf- DVT

 Wind – POD 1 to 3  Atelectasis & Pneumonia
 Water – POD 3 to 5 CA- UTI
 Walking- POD 4 to 8 DVT & PE
 Wound-POD 5 to 7 SSI
 Wonder drugs- anytime  Drug fever
 Physical examination- SSI, phlebitis; tenderness
on palpation of the abdomen, flank, or calf; or
cellulitis at the site of a central venous catheter.
 CBC, Urinalysis and culture, CXR, Blood culture.

POSTOPERATIVE FEVER
• Urinalysis showing more than 105
CFU/mL
(noncatheterized)  more than 103
CFU/mL
(catheterized)  UTI.
• Diagnosis of CR-BSI.
– Two simultaneous blood cultures or paired blood cultures
(i.e., simultaneous peripheral and central blood cultures)
– Peripheral blood cultures--bacteremia and isolation of 15
CFUs or 102 CFUs from an IV catheter  presence of CR-BSI.
– In tunneled catheters, a quantitative colony count that is 5-
fold to 10-fold higher in cultures drawn through the central
venous catheter is predictive of CR-BSI
– If paired cultures are obtained, positive culture more than 2
hours before peripheral culture (+)

• After removal of the catheter, the tip may be sent for
quantitative culture.
• Serial blood cultures and a transesophageal
echocardiogram are obtained in patients with S.
aureus bacteremia and valvular heart disease,
prosthetic valve, or new onset of heart murmur.
• Patients who continue to have fever, slow clinical
progress, and no discernible external source may
require CT to r/o intra abdominal source of
infection.

• PREVENTION-UTI
– Minimize duration of catheterization
– Maintenance of closed drainage system
– Changing catheter before blockage occurs if
prolongation required
– Use of silver alloy or impregnated catheters
– Use of protamine sulfate and chlorhexidine

• PREVENTION-CR-BSIs
– Maximal barrier precautions and infection control
practice during insertion.
– Educational programs- use and removal of catheter-
hand hygiene, skin antisepsis, full barrier precaution,
and stopping insertion when breaks in sterile
technique occur.
– Subclavian preferred over jugular and femoral veins
– Antiseptic-impregnated and antibiotic impregnated
catheters, routine use not recommended.

• TREATMENT
• Antipyretics
• Pneumonia suspect- empirical antibiotic therapy altered by culture results
• UTI
– Removal/replacement of catheter
– Broad spectrum antibiotics
• CR-BSI
– Removal of catheter with adjunctive antibiotic therapy,
– Alternative venous access.
– Single agent therapy- vancomycin, linezolid,emperical coveragof gram negative
bacilli and candida species.
– Catheter salvage- antibiotic lock therapy(catheter filled with antibiotic solution
for several hours)

RESPIRATORY COMPLICATIONS
• General Considerations
• Atelectasis and Pneumonia
• Aspiration Pneumonitis and Pneumonia
• Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
• Pulmonary Embolism and Venous
Thromboembolism

RESPIRATORY -General Considerations
• Factors -abnormal pulmonary physiology
– loss of functional residual capacity
• Abdominal distention
• Painful upper abdominal incision
• Obesity
• strong smoking history with associated COPD,
• Prolonged supine positioning
• fluid overload leading to pulmonary edema.
– Breathing pattern
– Vital Capacity reduced

– 2 types of respiratory failure
• Type 1.hypoxic-abnormal gas exchange at
alveolar level
– Ventilation perfusion mismatching and shunting
– Clinical conditions associated with- edema and sepsis
• Type 2.associated with hypercapnia and is
associated with low PaO2and high PaCO2
– Unable to eliminate Co2 adequately
– Associated with-excessive narcotic use, ARDS, altered
respiratory dynamics
RESPIRATORY -General Considerations

GENERAL CONSIDERATIONS
• History, patents with increased riskposteoanterior and
lateral CXR-baseline
• Polycythemia, chronic respiratory acidosisarterial blood gas
analysis
– PaCO2 <60mmHg-increased risk
– PaCO2 >45-50mmHg- perioperative morbidity high
• Spirometry- high risk patients before surgery
– FEV1 >2 liters-unlikely to have serious pulmonary
problems.
– FEV1 < 50% of the predicted value - likely to have
exertional dyspnea.
– If bronchodilator therapy demonstrates an improvement
in breathing patterns by >15%,consider bronchodilation.

ATELECTASIS AND PNEUMONIA
• Atelectasis- most common post op complication
• Pneumonia-most common nosocomial infection
• Anesthetic/abdominal incision/ postoperative
narcotics alveoli in the periphery
collapsepulmonary shunt may occurif
aggressive pulmonary toilet not donealveoli
remain collapsed buildup of secretions
secondarily infected with bacteria,
Pneumonia

PNEUMONIA
• Hospital acquired pneumonia-Pneumonia occurring more
than 48 hours after admission and without antecedent
signs of infection.
• Ventilator-associated pneumonia—pneumonia occurring
48 hours after but within 72 hours of the initiation of
ventilation.
• Health care–associated pneumonia - pneumonia
occurring in patients who were hospitalized in the last 90
days; patients in nursing facilities or frequenting a
hemodialysis unit; and patients who have received recent
antibiotics, chemotherapy, or wound care.

PNEUMONIA
• FACTORS ASSOCIATED WITH INCREASED RISK FOR PNEUMONIA
– Depressed immune status
– Concomitant disease
– Poor nutritional status
– Increased length of hospital stay
– Smoking
– Advanced age
– Uremia
– Alcohol consumption
– Prior antibiotic therapy
– Presence of an endotracheal,nasogastric (NG), or enteric tube
– Proton pump inhibitor (PPI) therapy.-Used to prevent stress ulceration,
PPI therapy increases colonization of the stomach with pathogenic
bacteria that can increase the risk of ventilator-associated pneumonia

• ORGANISMS ASSOCIATED HOSPITAL ACQUIRED
PNEUMONIA
– Streptococcus pneumoniae (colonizes upper airway)-
most common
– Haemophilus influenzae,
– Enterobacteriaceae spp. (E. coli, Klebsiella spp., and
Enterobacter spp.)
– S. aureus (mostly MRSA).
• Occasionally resistant to first generation
cephalosporins.

PNEUMONIA AND ATELECTASIS
DIAGNOSIS
 ATELECTASIS
– low-grade fever
– Malaise
– diminished breath sounds in the lower lung fields.
– With the use of incentive spirometry, deep breathing,
and coughing, most cases resolve without any difficulty
– If aggressive pulmonary toilet is not instituted pneumonia
 PNEUMONIA
– high fever
– mental confusion
– thick secretion with coughing
– leukocytosis
– CXR - infiltrates.
– may progress rapidly to respiratory failure and require intubation.

• Sputum for culture and sensitivity should be
sent immediately
• Quantitative cultures of the lower airways
obtained by blind tracheobronchial aspiration
• Bronchoscopically guided sampling
(bronchoalveolar lavage), or protected
specimen brush allow more targeted antibiotic
therapy.

PREVENTION AND TREATMENT
• Stop smoking for at least 1 week before surgery
• Treatment-COPD,asthma, and CHF - optimized.
• Pain control & proper pulmonary hygiene - post op.
• IPPV and chest physiotherapy
• Ventilator pt -semirecumbent position, oral hygiene.
• Chlorhexidine rinse or nasal gel,ET care, elimination
of secretions around the ET cuff, frequent suctioning
with a closed suction
• While awaiting culture results- emperical antibiotic
therapy

ASPIRATION PNEUMONITIS AND
ASPIRATION PNEUMONIA
• Aspiration of oropharyngeal or gastric contents
into the respiratory tract is a serious
complication of surgery.
• Aspiration pneumonitis(Mendelson syndrome)
is acute lung injury that results from the
inhalation of regurgitated gastric contents,
whereas aspiration pneumonia results from
the inhalation of oropharyngeal secretions that
are colonized by pathogenic bacteria.

PREDISPOSING FACTORS
• Impairment of the esophageal sphincters (upper and lower) and
laryngeal reflexes, altered GI motility
• Absence of preoperative fasting.
• Urgent surgery
• Altered levels of consciousness,
• GI and airway problems
• Cerebrovascular accidents -neurologic dysphagia and dysfunction of
the gastroesophageal junction.
• Anesthetic drugs reduce esophageal sphincter tone
• Patients with NG tubes or who are debilitated- difficulty in
swallowing and clearing airway.

• Pathophysiology of aspiration pneumonitis is related to
pulmonary intake of gastric contents at a low pH
associated with particulate matter.
• The severity of lung injury increases as the volume of
aspirate increases and its pH decreases.
• Often progresses rapidly, may require intubation soon
after the injury occurs, and later sets the stage for
bacterial infection.
• The pathophysiology of aspiration pneumonia is
related to bacteria gaining access to the lungs.

PRESENTATION AND DIAGNOSIS
• Associated vomiting
• May have received general anesthesia or had a NG tube
placed.
• Altered levels of consciousness.
• Initially- wheezing and labored respiration.
• Silent aspiration suggested by an infiltrate on a chest
radiograph or decreased PaO2.
• Other patients have cough, shortness of breath, and wheezing
that progress to pulmonary edema and ARDS.
• CXR- infiltrate in the posterior segments of the upper lobes
and the apical segments of the lower lobes.

• TREATMENT
– Reduce gastric contents, minimize regurgitation, and
protect the airway.
– Preoperative fasting
– Difficult airway -Awake fiber optic intubation
– In emergency situations -preoxygenation is
accomplished without lung inflation, and intubation is
performed after applying cricoid pressure during rapid-
sequence induction.
– Postoperatively- avoid the overuse of narcotics,
encourage the patient to ambulate, and feed cautiously

TREATMENT(cont)
• O2 ,Urgent CXR-bilateral, fluffy infiltrates.
• Oxygen saturation -face mask without excessively high work of
breathing, intubation may not be required.
• Patient’s oxygenation deteriorates and the work of breathing
increases-Increased RR Prompt intubation
• After intubation for suspected aspiration, suctioning the
bronchopulmonary tree confirms the diagnosis and removes
any particulate matter.
• Empirical antibiotics -aspiration pneumonitis that does not
resolve or improve within 48 hours of aspiration.
• Corticosteroid administration XXXXX
• Gram-negative cover-aspiration pneumonia.

PULMONARY EDEMA, ACUTE LUNG INJURY,
AND ADULT RESPIRATORY DISTRESS
SYNDROME
• Three of the most common manifestations of acute
respiratory failure are pulmonary edema, acute lung injury,
and ARDS.
• Pulmonary edema -accumulation of fluid in the alveoli-
oxygenation cannot take place-hypoxemia occurs.
– Increased work of breathing
– Increased respiratory rate
– Exaggerated use of muscles of respiration
• Acute lung injury and ARDS are associated with hypo-
oxygenation because of a pathophysiologic inflammatory
response-leads to the accumulation of fluid in the alveoli
as well as thickening in the space between the capillaries
and the alveoli.

SYNDROME
• Acute lung injury
– Pao2/fraction of inspired oxygen (FIO2) ratio of
less than 300
– Bilateral infiltrates on chest radiograph
– PCWP less than 18 mm hg
• ARDS
– Pao2/FIO2 ratio of less than 200
– bilateral infiltrates
– PCWP less than 18 mm hg.

PE,ALI,ARDS
PRESENTATION AND MANAGEMENT
• Frankly abnormal chest radiograph-invasive -
Swan-Ganz catheter for evaluation of PCWP.
• Elevated PCWP fluid restriction and
aggressive diuresis.
• Administration of oxygen via face mask in mild
cases and intubation in more severe cases is
also clinically indicated
• Diuresis and fluid restriction

PULMONARY EDEMA, ALI AND ARDS
• Tachypnea
• Dyspnea
• Increased work of breathing
• Cyanosis is associated with advanced hypoxia and is an
emergency.
• Auscultation-poor breath sounds,crackles and
occasionally with rales.
• Arterial blood gas analysis-low pao2 and high paco2.
• Administration of oxygen alone does not usually result
in improvement of hypoxia.

SYNDROME
• MANAGEMENT
– Immediate intubation plus careful administration of fluids
– Strategy involves maintaining the patient on the ventilator
with assisted breathing while the injured lung heals
– Initially placed on FIO2 of 100% and then weaned to 60%
as healing occurs.
– Tidal volume-6 to 8 ml/kg, peak pressure-35 cm H2O.
– Tidal volume is set at 10 to 12 ml/kg of body weight, and
the respiratory rate is chosen to produce a paco2 near 40
mm hg.
– Inspiratory-to-expiratory ratio is set at 1 : 2.

SYNDROME

PULMONARY EMBOLISM AND VENOUS
THROMBOEMBOLISM
• VTE comprises DVT and pulmonary embolism (PE).
• VTE is caused by a perturbation of the homeostatic coagulation
system induced by intimal injury, stasis of blood flow, and a
hypercoagulable state.
• The highest risk of VTE occurs in patients hospitalized for surgery.
• The prevalence of PE in patients with malignancy is 11%.
• Inflammatory bowel disease -5% (DVT) and 3%(PE)
• Major trauma- incidence-DVT exceeds 50%,with fatal emboli
occurring in 0.4% to 2% of cases
• Central venous catheter–related thromboses are more common
with femoral placement.

THROMBOEMBOLISM
• Most pulmonary emboli originate from an
existing DVT in the legs.
• iliofemoral venous system represents the site
from which most clinically significant
pulmonary emboli arise.
• Rare causes - fat embolus associated with
fractures of long bones and air embolism

THROMBOEMBOLISM

THROMBOEMBOLISM
• PRESENTATION AND DIAGNOSIS
• Approximately 5% to 10% of patients develop a massive PE
that results in hemodynamic instability(hypotension, with
or without shock) and death.
• Establishing the diagnosis of PE-
– Confirmatory tests(helical CT scan or pulmonary angiogram)
– Ancillary tests(venous duplex ultrasound [VUS] and D dimer
assay).
– Helical ct (spiral CT or CT pulmonary angiography)-high
specificity (92%) and sensitivity (86%)
• Pulmonary angiogram- gold standard test-visualizes the
arterial tree directly & detects intravascular filling defects.
– Less used-invasive & requires expertise

THROMBOEMBOLISM
• ECG-rapid, noninvasive, available bedside test
• Transthoracic echocardiography- hemodynamic
consequences of acute ventricular pressure overload—
– right ventricular dysfunction (hypokinesia and dilation),
– interventricular septal flattening and paradoxical motion,
– elevated tricuspid gradient,
– pulmonary hypertension,
– patent foramen ovale
• Dysfunction of the right ventricle occurs in 30% to 50%
of patients with PE who undergo echocardiography.

THROMBOEMBOLISM
• Venous CDFI-extremities -indirect test for
diagnosing PE.
• PE patients show findings consistent with DVT
• 80% ofpatients with PE have a DVT on the
venogram.
• D dimer levels are typically elevated in patients
with acute thromboembolism.
• Of the many D dimer tests,(ELISA) is the most
sensitive

THROMBOEMBOLISM
• Chest radiograph
• ECG
• Arterial blood gas analysis
• D dimer assay
• If leg symptoms are present-VUS
• If leg symptoms are absent-Spiral CT
• If spiral CT negative- clinical suspicion-
Angiogram

THROMBOEMBOLISM
• TREATMENT
• Medications
• Heparins- stops propogation of thrombus
• Fondaparinux- selectively inhibits factor Xa
• VKAs(eg. Warfarin)
• Thrombolytic agents(e.g., streptokinase,urokinase,
recombinant tissue plasminogen activator)

PROPHYLAXIS
• Low dose UFH 5000 U 3-4 hrs preop s/c & 8 hrly
• LMWH daily
NON PHARMACOLOGIC
THROMBOEMBOLISM

CARDIAC COMPLICATIONS
• Postoperative Hypertension
• Perioperative Ischemia and Infarction
• Cardiogenic Shock
• Postoperative Cardiac Arrhythmias
• Postoperative Heart Failure

POSTOPERATIVE HYPERTENSION
• The risk of hypertension is related to the type
of surgery performed and the presence of
perioperative hypertension.
• Preoperatively
– Essential hypertension
– Renovascular causes
– vasoactive tumors
• Intraoperatively, fluid overload and
pharmacologic agents may cause
hypertension.

• Postoperatively
– Pain
– Hypothermia
– Hypoxia
– Fluid overload in the postanesthesia period
– Discontinuation of long-term antihypertensive therapy before
surgery
– Intraabdominal bleeding
– Head trauma
– Clonidine withdrawal syndrome
– Pheochromocytoma crisis.

• PRESENTATION AND MANAGEMENT
– Routine pre operative workup
– Diastolic >110 mm Hg-assessed and treated
preoperatively.
– Long-term antihypertensive medications-continue
up to day of surgery.
– Oral clonidine  clonidine patch for at least 3
days before surgery.

• Intraoperatively
– Careful monitoring
– Avoid fluid overload, hypoxia and hypothermia
• Postoperative period,
– Pain control
– Long-term antihypertensive medications resumed.
– Unable to take oral medications
• Parenteral
– Beta blockers
– ACE inhibitors
– Calcium channel antagonists
– Diuretics
• Clonidine-transdermal patch

• HYPERTENSIVE CRISIS
– Severe elevation of blood pressure associated with organ
dysfunction—cerebral and subarachnoid hemorrhage and
stroke, acute cardiac events,renal dysfunction, and bleeding
from the operative wound.
– Carotid endarterectomy, aortic aneurysm surgery, and many
head and neck procedures.
• Diastolic hypertension (>110 mm Hg)-cardiac
complications
• Systolic hypertension (>160 mm Hg)-increased risk for
stroke and death.

• Medications-Rapid onset of action, Short half-life,
and Few autonomic side effects
– Nitroprusside and nitroglycerin (vasodilators)
– Labetalol and esmolol (beta blockers)
– Enalaprilat (useful for patients taking long-term ACE
inhibitors)
– Nicardipine (calcium channel blocker)
• Acute setting –Do not decrease blood pressure
>25% -avoid ischemic strokes and hypoperfusion
injury to other organs.

PERIOPERATIVE ISCHEMIA AND INFARCTION
• Approximately 30% of all patients undergoing
a surgical procedure have some degree of CAD
• Operation within 3 months of an infarction -
8% to 15% reinfarction rate; between 3 and 6
months postoperatively-3.5%.

• Myocardial ischemia and MI result from the
imbalance between myocardial oxygen supply and
demand.
• Primary causes that reduce myocardial perfusion
and oxygen supply
– Coronary artery-thrombus that develops on a disrupted
atherosclerotic plaque
– Dynamic obstruction caused by spasm of an epicardial
coronary artery or diseased blood vessel
– severe narrowing-progressive atherosclerosis.

• Secondary causes that increase myocardial oxygen
requirements, In the presence of Limited myocardial
perfusion
• Extrinsic cardiac factors that include
– Fever and tachycardia (increased myocardial oxygen demand),
– Hypotension (reduced coronary blood flow)
– Anemia
– Hypoxemia (reduced myocardial oxygen delivery).
• The increased circulating catecholamines associated with
surgical stress further increase myocardial oxygen demand.

• Presentation and Diagnosis
• Acute coronary syndrome comprises a
constellation of clinical symptoms that are
compatible with myocardial ischemia and
encompasses MI
– ST segment elevation myocardial infarction(STEMI)
and depression (Q wave and non–Q wave)
– Unstable angina/non–ST segment elevation
myocardial infarction (NSTEMI).

• Risk-greatest in the first 48 hours after surgery
• Chest pain radiating into the jaw and left arm
region—is often not present.
• Shortness of breath
• Increased heart rate
• Hypotension
• Respiratory failure

• Perioperative-often silent
– Shortness of breath (heart failure, respiratory
failure)
– Increased heart rate (arrhythmias)
– Change in mental status
– Excessive hyperglycemia in patients with diabetes.
• Many perioperative MIs are non–Q wave
NSTEMI.

• Periprocedural MI is associated with the release of
biomarkers of necrosis,
• MB isoenzymes of
– Creatine kinase (CK-MB)
– Troponins
• T (TnT),
• I (TnI),
• C (TnC).
• TnT and TnI are derived from heart-specific genes-
cardiac troponins-not present in healthy individuals

• Environment with Continuous ECG monitoring and
defibrillator capability.
• Biomarkers of myocardial necrosis-measured.
• CK-MB- less sensitive specific
• Troponins
– detected in blood by 2 to 4 hours
– Elevation-delayed for 8 to 12 hours.
– persist longer, for up to 5 to 14 days.
• Elevated cardiac troponin-above the 99th percentile of
normal in two or more blood samples-at least 6 hours apart
indicate the presence of myocardial necrosis.

PERIOPERATIVE ISCHEMIA AND
INFARCTION
• Perioperative
– beta blockers
– Careful intraoperative monitoring
– Maintenance of perioperative normothermia and
vital signs .
• Continued postoperative pharmacologic
management .

• Chronic stable angina
– Continue-antianginal medications
– Beta blockers are continued to the time of surgery
and thereafter.
– ECG-before, immediately after, and for 2 days after
surgery.
– Monitored for 48 hours after surgery
– High-risk patients- 5 days
– Cardiac enzyme levels

• Medical management of myocardial ischemia
and MI
– Immediate administrationof high-flow oxygen
– Transfer to the ICU
– Early consultation with a cardiologist.
• Immediate administration of beta blockers
(oral or IV, dose-titrated to decrease heart rate
to <70 beats/min) and aspirin (160 to 325 mg)

• Nitroglycerin (given as a continuous IV infusion
after a loading dose) alleviates pain and is
beneficial for patients with MI complicated by
heart failure or pulmonary edema.
• Systemic heparinization
• ACE inhibitors
• Thrombolytic therapy- Contraindicated
• No response to medical therapy-Angiography

CARDIOGENIC SHOCK
• 50% or more of left ventricular muscle mass is
irreversibly damaged reduction in
COhypoperfusion.
• CAUSES
– Ruptured papillary muscle or ventricular wall
– Aortic valvular insufficiency
– Mitral regurgitation,
– Ventricular septal defect.

CARDIOGENIC SHOCK
PRESENTATION AND MANAGEMENT
• Develops rapidly
• Marked by
• Hypotension
• respiratory failure
• Immediate –
– Mechanical ventilation- high FIO2
– Monitoring with a swan-ganz catheter .
• Intra-aortic balloon pumps
• Ventricular assist devices
• Coronary artery bypass
• Cardiac transplantation -gold standard--end-stage heart
failure.

POSTOPERATIVE CARDIAC ARRHYTHMIAS
CARDIAC ARRYTHMIAS
Tachyarrhythmia
Supraventricular
Sinus
Atrial
Nodal
Ventricular
Premature ventricular contraction
Ventricular tachycardia
Ventricular fibrillation
Bradyarrhythmia
Heart block

• Sinus tachycardia and atrial flutter - most
common types of tachyarrhythmia.
• Sinus tachycardia -caused by pain,fever,
hypovolemia, anemia, and anxiety
• Atrial flutter –electrolyte imbalance, history of
atrial fibrillation, COPD
• Ventricular ectopics-post operative-hypoxia,
acute hypokalemia, and hypercapnia

PRESENTATION
• Palpitations
• Chest pain
• Shortness of breath
• Dizziness
• Loss of consciousness
• Cardiac ischemia
• Hypotension

TREATMENT
• Control of the ventricular response
• Distinction between arrhythmias that traverse
the atrioventricular node(atrial fibrillation,
ectopic atrial tachycardia) from arrhythmias
that do not (ventricular tachycardia,
fibrillation)

TREATMENT
Cardiology consultation
Monitoring of patient on a telemetry floor or in ICU
12-lead ECG and long strip to differentiate between atrial and ventricular arrhythmia
Clinical assessment
• Vital signs
• Peripheral perfusion
• Cardiac ischemia and CHF
• Level of consciousness

TREATMENT-Tachyarrythmia
UNSTABLE
Cardioversion
STABLE
SUPRA
VENTRI
CULAR
TACHY
ARRHY
THMIA:
Beta
blocker
s
(esmol
ol),
ibutilid
e, or
alterna
tives
(e.g.,
digoxin,
calcium
channe
l
blocker
s,
amioda
rone)
PAROX
YSMAL
SUPRA
VENTRI
CULAR
TACHY
ARRHY
THMIA:
Vagal
stimula
tion or
adenos
ine;
digoxin,
amioda
rone,
or
calcium
channe
l
blocker
if
adenos
ine fails
MULTIF
OCAL
ATRIAL
TACHY
CARDI
A: Beta
blocker,
calcium
channe
l
blocker,
or
amioda
rone
VENTRI
CULAR
TACHY
CARDI
A:
Lidocai
ne,
procain
amide,
or
amioda
rone

TREATMENT OF BRADYARRHYTHMIA
AND HEART BLOCK
BRADYARRYTHMIA
• Sustained:
Atropine or β-
adrenergic
agonist
• Transient:
No therapy
HEART BLOCK
• Persistent high-grade second-
degree or third-degree block:
Insertion of permanent
pacemaker

POSTOPERATIVE HEART FAILURE
• Clinical syndrome characterized by any structural or
functional cardiac disorder that impairs the ability of the
ventricle to fill with or eject blood.
• CAUSES
– Perioperative MI
– Volume overload
– Hypertension
– Sepsis
– Occult cardiac valvular disease
– PE
– New-onset atrial fibrillation.

• PRESENTATION
– Shortness of breath
– Wheezing
– Tachycardia
– Narrow pulse pressure
– Low pressure or orthostatic hypotension
– Jugular venous distention
– Peripheral edema
– Rales
– General evidence of poor peripheral perfusion.

• PRESENTATION
– ECG
• MI
• Ventricular hypertrophy,
• Atrial enlargement
• Arrhythmias
– Chest radiograph
• Cardiomegaly
• Pulmonary edema
• Pleural effusion.

• TREATMENT
– Afterload reduction
• ACE inhibitors
– Preload reduction
• Nitrates (venodilator)
• Hydralazine (vasodilator)
– β-Adrenergic blockade
– Digoxin
– Volume overload
• Diuretics
– Hypertension or angina
• Calcium channel blockers

RENAL AND URINARY TRACT
COMPLICATIONS
• Urinary Retention
• Acute Renal Failure

URINARY RETENTION
• Inability to evacuate a urine-filled bladder- Causes
– MC-reversible abnormality -discoordination of the
trigone and detrusor muscles -increased pain and
postoperative discomfort.
– Perianal operations
– Hernia repair.
– Surgery for low rectal cancer -injury to the nervous
system
– Spinal procedures
– Vigorous IV administration of fluid.
– Benign prostatic hypertrophy

Presentation and Management
• Dull constant discomfort in the hypogastrium.
• Urgency and actual pain -as the retention worsens.
• Percussion just above the pubis – fullness and tenderness.
• Prevention in the population at greatest risk- older adults ,LAR
– Observe, Time since voiding -6-7 hrs
– Adequate management of pain
– Judicious administration of IV fluids
– Awareness of how much time has passed since the last voiding
• . General management
– Initial straight catheterization or placement of a Foley catheter,
– High-risk patients, cystoscopy and cystometry may be required.

Acute Renal Failure/Hospital-acquired renal insufficiency
• Sudden reduction in renal output that
results in the systemic accumulation of
nitrogenous wastes.
Major vascular procedures
(ruptured aneurysm)
Patients with advanced
diabetes undergoing
operations,
Major urologic operations,
Renal Transplant
Life-threatening trauma
Major blood loss, Major burn injuries,
Cardiopulmonary bypass
procedures,
Major abdominal cases
associated with septic shock,
Transfusion reactions, Multiorgan system failure

Types- ARF
• Oliguric renal failure
– urine in which volumes less than 480 mL are seen
in a day.
• Nonoliguric renal failure
– output exceeding 2 liters/day and associated with
large amounts of isosthenuric urine that clears no
toxins from the bloodstream.

ARF-Prevention
– Identification of patients with preexisting renal dysfunction;
– Avoid hypovolemia, hypotension, medications dec renal function;
– Judicious use of nephrotoxic drugs.
• Renal impairment- dose adjusted antibiotics -infections
• Contrast nephropathy -adequate hydration , premedication
with a free radical scavenger (e.g., N-acetylcysteine) or the
use of an alternative contrast agent (e.g., gadolinium).
• Renal hypoperfusion –Avoid-optimize CO and vol expn.
• Judicious administration of fluid - history of heart failure.
• Monitoring renal function -creatinine clearance
• Early intervention -postrenal obstruction and abdominal
compartment syndrome

• Anuria that suddenly develops postoperatively in an
otherwise healthy individual with no preexisting
renal disease is postrenal in nature until proven
otherwise.
• A kink in the Foley catheter
• obstruction must be cleared
• major pelvic surgery-ligation of the ureters is suspect.
• If renal ultrasound or a CT scan shows hydronephrosis,
immediate surgical treatment is indicated.

• Increase in the serum creatinine level,
• Decrease in creatinine clearance, and
• Urine output less than 400 mL/day (<20 mL/hr).
• Brown urine in the Foley bag in a trauma patient -
myoglobinuria
– rapid hydration
– diuresis
– alkalinization of the urine

Urine R/E, M/E
– Hyaline casts-hypoperfusion,
– Coarse granular casts - acute tubular necrosis.
– Lipoid casts -NSAIDinduced and contrast-induced
nephropathy
– White and red cell casts -pyelonephritis.

Prerenal vs renal azotemia
– Prerenal azotemia- Concentrating ability of the nephrons
Normal
• normal urine osmolality (>500 mOsm/liter )
• Normal fractional excretion of sodium( FENa <1%).
– Acute tubular necrosis-concentrating ability of the kidney is lost,
• urine osmolality equal to serum (350 mOsm )
• high urine sodium levels ( >50 mg/L,)
– Best laboratory test to discriminate prerenal from renal
azotemia- FENa.
• Prerenal azotemia, FENa is 1% or less,
• Renal azotemia-exceeds 3%.

Prerenal-Hypovolemeia vs cardiac?
• Diuretic vs more fluids
• History
• 1 litre in 20-30 min
• Foley- hourly U/O
• central venous pressure or Swan-Ganz catheter -left-sided
or right-sided heart filling pressure.
• CHF- diuretics, fluid restriction, and appropriate cardiac
medications
• Ultrasound - renal atrophy-chronic metabolic disease.

ARF- Treatment
• Management of fluid and electrolyte
imbalance
• Monitoring of fluid administration,
• Avoidance of nephrotoxic agents,
• Provision of adequate nutrition,
• Adjustment of doses of renally excreted
medications until recovery of renal function.

Hyperkalemia and fluid overload - most
urgent
• Hyperkalemia -sodium-potassium exchange resin,
insulin plus glucose, an aerosolized β2-adrenergic
agonist, and calcium gluconate.
• Insulin and β2-adrenergic agonists- shift potassium
intracellularly.
• Less severe hyperkalemia-ion exchange resin
(sodium polystyrene [Kayexalate]) enema
• Refractory hyperkalemia associated with metabolic
acidosis and rhabdomyolysis requires hemodialysis.

• β2-adrenergic agonist
– nebulizer containing 10 to 20 mg in 4 mL of saline over 10
minutes or
– an IV infusion containing 0.5 mg
• Calcium gluconate
– Hyperkalemia-associated cardiac irritability (prolonged P–R
interval or peaked T waves) treated urgently -10% calcium
gluconate solution over 15-minutes and simultaneous IV
administration of insulin and glucose (10-U IV bolus with
50 mL of a 50% dextrose solution, followed by
continuation of glucose to prevent hypoglycemia).
– Calcium gluconate -10 mL of a 10% solution over a 5-
minute- reduce arrhythmias.

• Phosphate levels
–Hypophosphatemia - induce rhabdomyolysis
and respiratory failure
• Treatment- oral administration of Fleet Phospho-
soda.
–Hyperphosphatemia with hypercalcemia-
increases the risk for calciphylaxis
• Treatment-administration of phosphorus binders
(calcium carbonate) or dialysis..

ENDOCRINE GLAND DYSFUNCTION
• Adrenal Insufficiency
• Hyperthyroid Crisis
• Hypothyroidism
• Syndrome of Inappropriate Antidiuretic
Hormone Secretion

ADRENAL INSUFFICIENCY
• Failure of the adrenal glands to produce
adequate glucocorticoids.
– Primary adrenal insufficiency-
• Addison disease-adrenal cortex-destroyed by cytotoxic
lymphocytes.
– Secondary adrenal insufficiency
• Long-term administration of Glucocorticoids.
Suppression
of
hypothalam
ic-pituitary
Adrena
l
atroph
Adrena
l
insuffici

• Acute adrenal insufficiency
– Abrupt cessation of pharmacologic doses of long-
term glucocorticoid therapy
– Surgical excision or destruction of the adrenal
gland(adrenal hemorrhage, necrosis, or
thrombosis in patients with sepsis or
antiphospholipid syndrome)
– Surgical excision/Destruction (postpartum
necrosis) of the pituitary gland.

• nonspecific—
– Fatigue,Weakness,Anorexia,Weightloss
– Orthostatic dizziness
– Abdominal pain,Diarrhea
– Depression,
– Hyponatremia
– Hypoglycemia
– Eosinophilia
– Decreased libido and potency.
– Hyperpigmentation -skin and mucous membranes

• HYPOTHALAMIC-PITUITARY-ADRENAL AXIS DISEASE
(HYPOPITUITARISM).
– Hypoadrenalism
– Decreased levels of corticotropin
– Manifestations of other hormone deficiencies
• Pallor
• loss of hair in androgen-dependent areas
• Oligomenorrhea
• diabetes insipidus
• hypothyroidism

• Laboratory test abnormalities
– Hyponatremia
– hyperkalemia,
– Acidosis
– Hypo or hyperglycemia
– Normocytic anemia
– Eosinophilia
– Lymphocytosis
• MORNING PLASMA CORTISOL CONCENTRATION
– >19 μg/dL -rules out adrenal insufficiency
– <3μg/dL - indicates the presence of adrenal insufficiency.

RAPID ADENOCORTICOTROPIC HORMONE STIMULATION TEST
IN PATIENTS WITH ADRENAL ISUFFICIENCY
• Determine baseline serum cortisol level.
• Give IV (or IM) cosyntropin, 250 μg.
• Measure serum cortisol levels 30 to 60 minutes after cosyntropin is given.
• Results
• Normal adrenal function:
• Basal or postcorticotropin plasma cortisol concentration is at least 18
μg/dL or preferably 20 μg/dL.
• Primary adrenal insufficiency
• Cortisol secretion is not increased.
• Severe secondary adrenal insufficiency
• Cortisol levels increase a little or not at all because of adrenocortical
atrophy.

• MRI- Evaluation of pituitary hypothalamic
region.
• CT- Evaluate adrenal glands

TREATMENT
• Stress dose of hydrocortisone (100 mg)-with
induction of anesthesia.
• For minor surgical procedures-maintenance dose
-continued postoperatively.
• For major surgical procedures, stress dose (100
mg) is continued every 8 hours until the patient
is stable or free of complications and then
tapered to the usual maintenance dose.

TREATMENT
• Symptomatic patients are treated with
hydrocortisone or cortisone.
• Fludrocortisone (substitute for aldosterone) is also
administered to patients with primary disease.
• Treatment of functional acute adrenal insufficiency
involves immediate, rapid administration of high-
dose hydrocortisone or methylprednisolone

HYPERTHYROID CRISIS
• Hyperthyroidism-sustained increase in the
synthesis of thyroid hormones
• Thyrotoxicosis- clinical syndrome that
results from an abnormal elevation of
circulating levels of thyroid hormone,
regardless of cause.
• Medical emergency
– Thyrotoxic patients with toxic adenoma or toxic
multinodular goitre
– Graves disease.

HYPERTHYROID CRISIS
• Precipitated by stressfull event
• Hyperthyroidism
– Nervousness
– Fatigue
– Palpitations
– Heat intolerance
– Weight loss
– Atrial fibrillation (in older patients)
– Ophthalmopathy-eyelid retraction or lag,
periorbital edema, and proptosis

HYPERTHYROID CRISIS
• Sudden onset
• Accentuation of the symptoms and signs of thyrotoxicosis and
organ system dysfunction
– Hyperpyrexia
– Tachycardia
– Out of proportion to fever
– Dehydration
– Collapse
– Central nervous system dysfunction (delirium, psychosis,
seizure, coma)
– Cardiac manifestations
– GI symptoms
– Liver dysfunction.

HYPERTHYROID CRISIS
DIAGNOSIS
• Elevated levels of thyroid hormones
• Suppresed levels of TSH
• Thyroid scintigraphy with technetium-99m
pertechnetate or iodine-123 (123I)
–Graves disease-diffuse uptake
–Plummer disease-inhomogeneous pattern
with hot, cold, and warm areas
–Goetsch disease (toxic solitary nodule)-
intense activity in the area of the nodule,
with suppression of paranodular tissue.

HYPERTHYROID CRISIS- MANAGEMENT

HYPOTHYROIDISM
• Low systemic levels of
thyroid hormones
• Exacerbated-preexisting
chronic hypothyroidism or as
a result of severe stress.

HYPOTHYROIDISM
Hypothyroidism
Primary
Eg.Surgical removal, ablation, disease of the thyroid gland)
Secondary
(eg-Hypopituitarism)
Tertiary
(eg, Hypothalamic disease)

HYPOTHYROIDISM
• ECG
– Bradycardia
– Low voltage
– Prolonged P–R, QRS, and Q–T intervals.
• Primary hypothyroidism
– Serum total T4, free T4, and free T3 levels-low
– TSH level-elevated
• Secondary disease
– TSH level-low
– Free T4 index, and free T3-low.

HYPOTHYROIDISM
TREATMENT
• Replacement hormone therapy continued
till euthyroid state reached
• Myxedema coma or patients showing
clinical signs of significant hypothyroidism
–Immediately treated with thyroid
hormone
–IV administration of hydrocortisone, to
avoid an addisonian crisis
–IV levothyroxine or T3 may be given until
oral ingestion is possible.

SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE SECRETION
• Most common cause of chronic normovolemic
hyponatremia(serum sodium<135 mmol/liter)
• Remains hyponatremic despite all attempts to correct the
imbalance in the presence of persistent antidiuretic activity
from elevated arginine vasopressin levels.
• Predisposing factors
– Trauma
– Stroke
– Antidiuretic hormone– producing tumors
– Drugs (ACE inhibitors, dopamine, nsaids)
– Pulmonary conditions.

• PRESENTATION
–Anorexia
–Nausea
–Vomiting
–Obtundation
–Lethargy
• With more rapid onset
–seizures, coma, and death can result.

PRESENTATION
• The cardinal criteria of SIADH
–Hyponatremia with hypotonicity of plasma
–Urine osmolality in excess of plasma
osmolality
–Increased renal sodium excretion
–Absence of edema or volume depletion
–Normal renal function.

TREATMENT
• Treatment of the underlying disease process
• Treatment of hyponatremia- removal of excess water
• Fluid restriction is the mainstay of management
• Correction –rate of 0.5 mmol/ liter/hr until the serum
sodium concentration is 125 mg/dL or higher.
• Rapid correction-serious permanent neurologic damage.
• Diuretics

GASTROINTESTINAL COMPLICATIONS
• Ileus and Early Postoperative Bowel Obstruction
• Acute Abdominal Compartment Syndrome
• Postoperative Gastrointestinal Bleeding
• Stomal Complications
• Clostridium Difficile Colitis
• Anastomotic Leak
• Intestinal Fistulas
• Pancreatic Fistulas

Ileus and Early Postoperative Bowel
Obstruction
• Early postoperative bowel obstruction - within 30
days after surgery
– Functional (i.e., ileus), -inhibition of propulsive
bowel activity
• Primary or postoperative ileus- occurs immediately
after surgery in the absence of precipitating factors
and resolves within 2 to 4 days
• Secondary, adynamic, or paralytic ileus- result of a
precipitating factor and associated with a delay in
return of bowel
– Mechanical (Partial or complete, high or low,
closed vs open loop)
• luminal, mural, or extraintestinal barrier

• Surgical stress and manipulation of the bowel result in
sustained inhibitory sympathetic activity results in
suppression of the neuromuscular apparatus.
• Opiates and opioid peptides in the enteric nervous
system suppress neuronal excitability.
• After resection and reanastomosis of the small bowel,
the distal part of the bowel does not react to the
pacemaker and the frequency of contractions decreases.

Paralytic/Adynamic Ileus- Causes

Mechanical Obstruction-Causes
• Adhesions (92%)
• Phlegmon or abscess- Anastamotic leak,
Iatrogenic Injury
• Internal hernia
• Intestinal ischemia
• Intussusception(rare)

Normal return of bowel activity
• Small bowel motility - within several hours
• Gastric motility- within 24 to 48 hours
• Colonic motility-within 48 to 72 hours.
• Bowel sounds, flatus, and bowel movements.
• Gastric dilation and vomiting

Presentation
• Cause, degree and
• Stasis and progressive accumulation of gastric
and intestinal secretions and gas-bowel loses
its tone and dilate- abdominal distention,
pain, nausea and vomiting, and obstipation

Adynamic Vs Mechanical
• Adynamic ileus
– diffuse discomfort but no sharp colicky pain
– distended abdomen.
– quiet abdomen, with few bowel sounds
• Mechanical obstruction
– high-pitched, tinkling sounds
– Fever, tachycardia,
– +/- manifestations of hypovolemia, and sepsis

• In adynamic ileus, abdominal radiographs reveal
diffusely dilated bowel throughout the intestinal
tract, with air in the colon and rectum.
• With mechanical bowel obstruction, there is
small bowel dilation with air-fluid levels and
thickened valvulae conniventes in the bowel
proximal to the point of obstruction and little or
no gas in the bowel distal to the obstruction

• Measures to prevent ileus intraop
– Handle the tissues gently
– limit peritoneal dissection to only what is
essential.
– The bowel must not be allowed to desiccate by
prolonged exposure to air without protection
– Anti-adhesion barriers- an oxidized cellulose
product and a product that is a combination of
sodium hyaluronate and carboxymethyl cellulose.

Post op
• Electrolyte imbalance
• Alternative to narcotics- NSAIDs, Epidural
• RT ?

• Three step approach for post op ileus
resuscitation
investigation
surgical intervention.
• Emergency relaparotomy is performed if there is a
closed loop, high-grade, or complicated small bowel
obstruction, intussusception, or peritonitis.
• Adynamic ileus and partial mechanical-waiting
expectantly for resolution(7-14 d)

Acute Abdominal Compartment Syndrome
• Abdominal compartment syndrome (ACS) describes increasing
organ dysfunction or failure as a result of IAH.
• IAH
– consistent increased IAP value higher than 12 mm Hg
– minimum of 3 measurements 4 to 6 hours apart,
– measured at the end of expiration
• ACS
– IAP -20 mm Hg or greater,
– abdominal perfusion pressure < 50 mm Hg (at least 3 measurements
performed 1 to 3 hours apart)
– (abdominal perfusion pressure = mean arterial pressure − IAP)
– associated with failure of one or more organ systems

• Primary ACS develops as a result of pathologic IAH caused
by intra-abdominal pathology and
• Secondary ACS develops in the absence of intra-
abdominal primary pathology, injury.
• Primary ACS is most commonly encountered in victims of
multiple trauma and after damage control surgery due to
bowel edema and contamination, continued bleeding,
coagulopathy, packing used to control bleeding, capillary
leak, and massive fluid resuscitation and transfusion.

• In nontrauma patients, IAH and possibly primary ACS
have been reported to occur in patients with
– Ascites
– Retroperitoneal hemorrhage
– Pancreatitis
– Pneumoperitoneum
– After reduction of chronic hernias
– Repair of ruptured abdominal aortic aneurysm,
– Complex abdominal procedures, and liver
transplantation

• Secondary ACS is in part iatrogenic and
commonly encountered in patients with
–shock requiring aggressive fluid
resuscitation with crystalloids
–Thermally injured and shock trauma victims
–Critically ill hypothermic
–septic patients
–Sustained cardiac arrest

Diagnosing ACS
• Respiratory difficulty, Oliguria ,high filling pressures
and vasopressor therapy is required. The abdomen
becomes distended and tense, and neurologic
deterioration may occur.
• Use of the urinary bladder catheter -gold std-
indirectly IAP.
– GI (IAP <10 to 15 cm H2O),
– GII (IAP <16 to 25 cm H2O)
– GIII (IAP <26 to 35 cm H2O)
– GIV (IAP >36 cm H2O).

• The prevention of primary ACS -by leaving the
peritoneal cavity open in patients at risk for IAH and
after high-risk surgical procedures.
• Patients at risk for secondary ACS receiving crystalloid
resuscitation must be monitored closely.
• The decision surgical intervention is not based on IAH
alone but rather on the presence of organ dysfunction
in association with IAH.

• Decompression leads to reduction of IAH,
severe hypotension and abrupt increase in the
true tidal volume delivered to the patient,
with washout of the byproducts of anaerobic
metabolism
• This results in respiratory alkalosis

• Decrease in effective preload
• Hence, decompression is performed after
adequate preload with volume has been
established.

Postoperative Gastrointestinal Bleeding
• Possible sources in the stomach include peptic
ulcer disease, stress erosion, a Mallory-Weiss
tear, and gastric varices
• In the small intestine, arteriovenous
malformations and bleeding from an
anastomosis
• In the large intestine, anastomotic hemorrhage,
diverticulosis, arteriovenous malformations

Risk Factors for Development of Stress Erosions
• Multiple trauma
• Head injury
• Major burns
• Clotting abnormalities
• Severe sepsis
• Systemic inflammatory response syndrome
• Cardiac bypass
• Intracranial operations

The basic principles of management of postoperative GI bleeding
1. Fluid resuscitation and restoration of
intravascular volume
2. Checking and monitoring clotting parameters and
correcting abnormalities, as needed
3. Identification and treatment of aggravating
factors
4. Transfusion of blood products
5. Identification and treatment of the source of the
bleeding

Stomal Complications
• Colorectal, intestinal and
urologic diseases.
• Ischemic necrosis - impaired
perfusion to terminal portion
of the bowel - a tight aperture,
overzealous trimming of
mesentery, or mesenteric
tension.
• Stomal retraction - tension on
the bowel or ischemic necrosis
of the stoma.
• Late retraction -increased
thickness of the abdominal
wall with weight gain.

• Stomal prolapse can result in incomplete
diversion of stool, interfere with the stoma
appliance, lead to leakage of stool
• A peristomal fistula is often a sign of Crohn’s
disease
• Pyoderma gangrenosa may develop in patients
with inflammatory bowel disease
• Parastomal varices may develop in patients with
liver disease.

Technical aspects of Stoma Construction

Clostridium difficile Colitis
• It is an inflammatory bowel disease caused by
toxins produced by unopposed proliferation of
C. difficile
• cephalosporins, clindamycin, and ampicillin-
amoxicillin were most commonly associated
with CDI

• Presents with watery diarrhea
• The stools are foul-smelling and may be
positive for the presence of occult blood
• In severe colitis, the diarrhea becomes
associated with abdominal cramps and
anorexia, abdominal tenderness, dehydration,
tachycardia, a raised leukocyte count

• Pseudomembranous colitis is the more dramatic
form of the disease and develops in 40% of patients
• Antibiotic of choice is metronidazole
• Colectomy is indicated when medical treatment
fails or when the patient develops hemodynamic
instability, fulminant disease, toxic megacolon, or
peritonitis.

Anastomotic leak
• It is leakage of intestinal contents after resection and
anastomosis
• The level of the anastomosis in the GI tract is
important.
• Small bowel, ileocolic, and ileorectal anastomoses are
considered safe
• Esophageal, pancreaticoenteric, and colorectal
anastomoses are considered high risk for leakage.
• In the esophagus, lack of serosa appears to be a
significant contributing factor.

• In the rectum, the highest leak rate is found in
anastomoses in the distal rectum, 6 to 8 cm from
the anal verge.
• Adequate microcirculation at the resection margins
is crucial for the healing of any anastomosis.
• Intraluminal distention is believed to be
responsible for rupture of an anastomosis.

Construction of an anastomosis that is at low risk for disruption
• Adequate exposure, gentle handling of tissues,
aseptic precaution,and meticulous, careful
dissection
• Adequate mobilization -tension-free anastomosis
• Correct technical placement of sutures or staples
with little variance
• Matching of the lumens
• Preservation of the blood supply to the ends

• Factors interfering with the perianastomotic
microcirculation include
– Smoking
– Hypertension
– locally enhanced coagulation activity as a result
of surgical trauma
– perianastomotic hematoma
– presence of macrovascular disease
–Infection

• The early warning signs of anastomotic leak are
malaise, fever, abdominal pain, ileus, localized
erythema around the surgical incision, and
leukocytosis.
• There may be an initial excessive drainage from the
surgical wound or surgical wound dehiscence and/or
evisceration.
• Sepsis is a prominent feature of anastomotic leakage
and results from diffuse peritonitis or localized
abscess

• Once an anastomotic leak is suspected or
diagnosed, resuscitation is started immediately
• Oral intake is stopped and the bowel is put at rest
• Reoperation is indicated if there is diffuse
peritonitis, intraabdominal hemorrhage,
suspected intestinal ischemia, major wound
disruption, or evisceration

Intestinal Fistulas
• A fistula represents an abnormal
communication between two epithelialized
surfaces, one of which is a hollow organ.
• In the GI tract, a fistula may develop between
any two digestive organs or between a hollow
organ and the skin

• They commonly occur as the result of
–Anastomotic breakdown
–Crohn’s disease
–Radiation enteritis
–Distal obstruction
–Abscess or peritonitis

• Enterocutaneous fistulas are usually
associated with a triad of sepsis, fluid and
electrolyte imbalance, and malnutrition
• Fistula -high or low output on the basis of the
volume of discharge in 24 hours.
– low output (<200 mL/24 hr)
– Moderate output (200 to 500 mL/24 hr),
– High output (>500 mL/24 hr).

• The first step in the management of a GI fistula is
to prevent its occurrence
• Oral intake is stopped and the bowel is put at rest
• Management involves resuscitation, TPN,
correction of electrolyte imbalances, and
transfusions

Factors affecting healing of fistulas

HEPATOBILIARY COMPLICATIONS
• Bile Duct Injuries

BILE DUCT INJURIES
• Cholecystectomy accounts for most postoperative
biliary injuries and strictures.
• Bile leak may-bile duct injury, cystic duct stump leak,
divided accessory duct, or injury to the intestine.
• Acute cholecystitis, a foreshortened cystic duct,
anomalies of the biliary tree, hemorrhage from injury
to the cystic or hepatic artery, failure to define
anatomy of calot
• The most common injury sustained during the
laparoscopic procedure is complete transection at or
below the hepatic duct bifurcation

• Bile leakaccumulate in the subhepatic spaceform
biloma or seep into the peritoneal cavitybile ascites
– Right upper quadrant pain
– Fever
– Nausea
– Abdominal distention
– Malaise.
• Bile-intraoperatively placed drain-manifest as a bile
leak
– Leukocytosis
– Slightly elevated bilirubin level.

DIAGNOSIS
• Nuclear medicine imaging-presence of a leak or
obstruction
• CT scan-identify bile collections or ascites
• ERCP-define the type and level of injury accurately.
• Percutaneous transhepatic cholangiography-define
the proximal anatomy and site of injury
• MRCP-testof choice-late strictures and define the
bile duct anatomy

TREATMENT- Intraop
• Proper surgical technique and adequate
identification of the anatomy
• The cystic duct and artery to be divided when the
anatomy is clearly delineated.
• Avoid Excessive traction on the gallbladder-tenting
of the common duct.
• Bleeding in the area of the cystic duct-blind clipping
and cautery must avoided
• Intraoperative cholangiography helps identify the
anatomy and any injuries

• TREATMENT(CONT)
• Intraoperative diagnosis of leak- immediate
repair
A
n
a
c
c
e
s
s
o
r
y
d
u
c
t
l
i
g
a
t
e
d
H
i
g
h
i
n
j
u
r
y
c
a
n
b
e
r
e
p
a
i
r
e
d
w
i
t
h
a
r
o
u
e
x
-
e
n
-
Y
b
i
l
i
a
r
y
e
n
t
e
r
i
c
a
n
a
s
t
o
m
o
s
i
s

TREATMENT-POSTOPERATIVE PERIOD
• Biloma-drained percutaneously, and a
sphincterotomy is performed or a stent
is placed.
• Major obstruction of bile duct, major
injury, suspicion of bowel injury-
SURGICAL REPAIR

Adequate
resuscitati
on
Administra
tion of
antibiotics
Watch for a few
days to ensure
that they are not
septic at the time
of the operation
If there is
evidence of
adequate control
of the leak
Wait 5 to 7 days
for
inflammation in
the area to
subside
Identify
source of the
bile
extravasation
When it has been
ascertained that there
is tissue with good
integrity
Roux-en-y limb can be
anastomosed to the
common bile duct.
Multiple
drains are left
around the
site of the
repair.

NEUROLOGIC COMPLICATIONS
• Delirium, Cognitive Disorder, and Psychosis
• Seizure Disorders
• Stroke and Transient Ischemic Attacks

DELIRIUM, COGNITIVE DISORDER, AND
PSYCHOSIS
• Delirium- a state of acute confusion

DELIRIUM-PRESENTATION AND DIAGNOSIS
– Acutely agitated, uncooperative, and confused.
– Previous psychiatric disorder-withdrawn and
depressed.
– Noncommunicative and emotionally flat
– Withdraw from any emotional exchange.
– Altered level of consciousness
– Changes in cognition.
– Reduced ability to focus
– Decreased levels of awareness
– Difficulty with attention
– Symptoms worsen at night

PSYCHOSIS
PRECIPITATING FACTORS
• Postoperative anemia (secondary to acute blood loss)
• Electrolyte imbalance
• Sepsis
• Malnutrition
• Bladder catheterization
• Physical restraints
• Extended duration of anesthesia
• Infection
• Respiratory complications

PSYCHOSIS
DELIRIUM TREMENS
• The most immediately threatening disorder encountered by
physicians
• Occurs 48 hours to 14 days after acute alcohol withdrawal.
• Extreme autonomic hyperactivity
• Fever
• Tremor
• Tachycardia
• Confusion, psychosis, agitation, and seizures.
• Because of the serious underlying nutritional and medical
deficiencies, these patients have moderately high mortality,

PSYCHOSIS
TREATMENT
Treatment of patients with acute confusion or a sudden
change in behavior after surgery requires the following:
1. Recognition of the disorder
2. Close observation and monitoring
3. Identification and elimination of the precipitating factor
4. Treatment of any associated laboratory abnormalities
5. Selective use of imaging or other studies to rule out an
organic brain lesion
6. Application of measures to protect the patient and staff
7. Treatment

DELIRIUM, COGNITIVE DISORDER,
AND PSYCHOSIS
MEDICAL THERAPY
• Haloperidol, a neuroleptic (0.5 to 2 mg, given iv or im
to achieve a rapid effect and then orally for
maintenance therapy).
• Benzodiazepines are the DOC for acute alcohol
withdrawal.
• Other medications
– Beta blockers (to control autonomic
manifestations)
– Clonidine (to control HTN) are given in addition to
benzodiazepine to patients with acute alcohol
withdrawal.

SEIZURE DISORDERS
Caused by paroxysmal electrical discharges from the
cerebral cortex
• PRIMARY CAUSES
– Intracranial tumor
– Hemorrhage
– Trauma
– Idiopathic seizure activity.
• SECONDARY CAUSES
– Metabolic derangement
– Sepsis
– Systemic disease processes
– Pharmacologic agents

SEIZURE DISORDERS
• PRESENTATION
–Convulsions
–Rhythmic myoclonic activity
–Loss of consciousness
–Change in mental status
–Fecal and urinary incontinence
–Lack of neurologic responsiveness
–Postevent amnesia.

SEIZURE DISORDERS
MANAGEMENT
• Administration of IV benzodiazepine- immediate care
• Phenytoin (Dilantin)-most commonly used
anticonvulsant for new-onset generalized or focal
seizures
• Phenobarbital-because of sedation-it is not an agent of
choice.
• Status epilepticus- carbamazepine (Tegretol) and
valproic acid.
• Refractory to other drugs-Gabapentin

SEIZURE DISORDERS
WORK UP
• Detailed history
• Physical examination
• History of previous medication and drug use
• WBC count to rule out occult infection
• Electrolyte and metabolic assessment.
• CT or MRI is indicated-new-onset seizure
activity(Tumours)
• Electroencephalogram-abnormal waveform activity.

STROKE AND TRANSIENT ISCHEMIC ATTACKS
Postoperative strokes
Ischemic strokes
1.perioperative hypotension
2.overzealous control of hypertension
3.cardioemboli in patients with atrial
fibrillation.
Hemorrhagic strokes
1.Therapy with anticoagulants
2.Factors related to coagulation disorders,
such as chronic abuse of alcohol, AIDS,
cocaine use, bleeding diathesis
3.preexisting cerebrovascular anomalies

• PRESENTATION AND MANAGEMENT
• A focal alteration in motor function, alteration in mental
status, aphasia, or occasionally unresponsiveness
• Prevention of a perioperative stroke
– Hypertension-adequate treatment
– Overzealous correction-avoided.
– Atrial fibrillation-prophylaxis with anticoagulants.
– High-risk surgical procedure (e.G., Carotid endarterectomy)-
monitored intraoperatively- transcranial doppler and
electroencephalography.

TREATMENT
• IV line placed and be monitored for cardiac arrhythmias.
• Coagulation parameters-presence of a coagulopathy
• Blood culture-bacteremia and bacterial endocarditis.
• CT scan or MRI- distinguish between hemorrhagic and
ischemic stroke
• Hypertensive hemorrhagic stroke-control of the hypertension,
• Embolic stroke-anticoagulation
• Hemorrhagic stroke- reversal of the coagulopathy with
protamine if secondary to heparin or platelet transfusion if
secondary to antiplatelet therapy.
• Mannitol and dexamethasone are given to reduce cerebral
swelling.

• Surgical intervention-localized hematoma or
vascular anomaly
• Thrombolytic therapy (recombinant tissue
plasminogen activator) -restoring cerebral blood
flow and minimizing brain injury-instituted early
after the onset.
• low-dose aspirin therapy-standard-acute ischemic
infarction
• antiplatelet agents (e.g., clopidogrel bisulfate,
ticlopidine hydrochloride) are added in patients
who continue to have symptoms.

EAR, NOSE, AND THROAT COMPLICATIONS
• Epistaxis
• Acute Hearing Loss
• Nosocomial Sinusitis
• Parotitis

Prevention of post operative complications

“Nothing is ever so bad that it cant get worse”
– Guttuso’s extension of Murphys law
“Pick well, Cut well, they will do well!”
THANK YOU 

Post Op complications in general surgery

More Related Content

Similar to Post Op complications in general surgery

Recently uploaded

Post Op complications in general surgery

Editor's Notes